• Journal of Life Science
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• v.11 no.4
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• pp.346-353
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• 2001

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) a prototype of the highly toxid halogenated arylhydrocarbons, bioaccumulates in the food chain and induces a complex spectrum of pathological responses. However, its effect on the nerve system is relatively not well studied. In this study we evaluated TCDDs cytotoxicity on the cortical cell and investigated its effect on the expression 2,3-cyclic nucleotide 3-phosphodiesterase(CNPase), a marker for oilgodendrocytes, The survival rates of 4 DIV cortical cells, that are dissociated from E18 rat cortex and maintained in the presence of TCDD, were 88.8, 83.6, 78.5, and 78.6%(5,10, 20 and 50 nM, respectively) where the reduction in 20 and 50mM TCDD were statistically very significant(p<0.01). Imunocytochemistry of cultured cells revealed that the intensities of immunostaining with an anti-CNP1&2 antibody depended on the concentrations of the toxin. Immunoblot analysis also showed differential expression of CNP1 and CNP2 in the presence of TCDD; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 in the presence if TDCC; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 fluctuated with the TCDD concentration. These results indicated that CNP1 and 2 are differentially regulated by TCDD, implying the functions of oligodendrocytes are modulated by the toxin.

• 대한생식의학회:학술대회논문집
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• 2007.11a
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• pp.99-99
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• 2007

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.125-125
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• 2002

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.129-129
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• 2002

• Environmental Analysis Health and Toxicology
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• v.25 no.3
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• pp.241-251
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• 2010

Crucian carp (Carassius auratus) has been used as the sentinel species for POPs (Persistent Organic Pollutants) monitoring in aquatic environment. However, there is little information for dioxin toxicity and especially, early life stage toxicity in crucian carp have been never carried out. In this study, we investigated several toxic effects for 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in fertilized egg obtained by natural fertilization from crucian carp. The embryos at 3 h post-fertilization (hpf) were treated with 0.039, 0.156, 0.625, and 2.5 (${\mu}g/L$) TCDD by waterborne exposure for 60 minutes and changed with fresh water 2 times per day. Fertilized eggs started hatching at 51 hpf and TCDD exposed embryo showed decrease of hatching rate in a dose-dependent manner at 75 hpf. Pericardial edema was continuously observed in larvae exposed to TCDD from hatching start time (51 hpf), followed by the onset of mortality. In addition, AhR-related gene, CYP1A was clearly increased by TCDD in a dose dependent manner. These results indicated that fertilized eggs obtained from crucian carp have the TCDD related gene regulation and a distinct TCDD developmental toxicity syndrome by TCDD exposure. Therefore, we suggested that early life stage test in crucian carp could be used as test methods on dioxins toxicity.

• Proceedings of the Korea Society of Environmental Biology Conference
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• 2001.12a
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• pp.127-127
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• 2001

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.118.1-118.1
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• 2003

A growing body of scientific research indicates that man-made chemicals (xenobiotics) may interfere with the normal functioning of endocrine, or hormone systems. These endocrine disruptors may cause a variety of problems with development, behavior, and reproduction. Amongst the xenobiotics the World Health Organization classed 2, 3, 7, 8-TCDD as a "known" human carcinogen. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.179-179
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• 2003

2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanisms of TCDD-induced carcinogenesis are poorly understood, it considered to be non-genotoxic and tumor promoter. In this study, we investigated the tumor promotion effect of TCDD on the two-stage skin chemical carcinogenesis using hairless mouse (SKH1).(omitted)

• Journal of Microbiology and Biotechnology
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• v.10 no.3
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• pp.281-286
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• 2000

2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD), a ubiquitous environmental contaminant, causes a variety of adverse effects on the male reproductive system in rats. The effect of green tea extract (GTE) was investigated on the testicular function in Spragure-Dawley rats after a single exposure of 10$\mu\textrm{g}$ TCDD/kg body weight. The exposure of rat to TCDD significantly increased the weights of the epididymis and ventral prostate, yet significantly decresed the weight of the seminal vesicle when compared to the controls (p<0.05). In a combined treatment of TCDD with GTE, the organ weight changes caused by TCDD treatment disappeared. Significant decreases in sperm motility and sperm numbers were observed in the TCDD-treated rats, when compared to the control (p<0.05). GTE treatment reversed the decrease of sperm motility and sperm numbers caused by TCDD. There were no differences in sperm morphology, histological changes of the reproductive organs, and spermatogenesis between all the treated groups. In the ventral prostate and seminal vesicle, TCDD increased the CYP1A1 mRNA level, however, it did not affect the estrogen receptor $\beta$ (ER-$\beta$) mRNA level. GTE treatment did not influence the effect of TCDD on the levels of CYP1A1 and Er-$\beta$ mRNA. These results seem to indicate that green tea protects the testicular function against TCDD-induced reproductive toxicity, not because of a receptor-mediated mechanism but rather due to a secondary change of testes or accessory sex organs.

• Toxicological Research
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• v.19 no.4
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• pp.325-330
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• 2003

The effects of estrogen on apoptosis induced by 2,3,7,8-tetrachlorodibenzo-p-doxin (TCDD) were examined in cultured MCF-7 cells. TCDD stimulated apoptosis and inhibited the expression of bcl-2 gene in MCF-7 cells grown in the media supplemented with 10% fetal bovine serum. However, TCDD failed to induce apoptosis if cells were grown in the media deprived of all estrogen-like compounds. Removal of estrogen-like compounds from the growth media also led to the activation of bcl-2 gene expression in cells treated with TCDD. Combined treatment of estrogen with TCDD abrogated the binding of Aryl hydrocarbon Receptor (AhR)-TCDD complex to Dioxin response element (DRE) of bcl-2 gene leading to the inhibition of bcl-2 gene expression as well as stimulation of apoptosis. The present study suggests that the binding of estrogen receptor (ER)-estrogen complex to the estrogen responsive element (E) interferes with the binding of AhR- TCDD complex to the DRE and inhibits the bcl-2 expression.